MicroRNAs (miRNAs) and Long Non-Coding RNAs (lncRNAs) as New Tools for Cancer Therapy: First Steps from Bench to Bedside

Ratti, Margherita; Lampis, Andrea; Ghidini, Michele; Salati, Massimiliano; Mirchev, Milko; Valeri, Nicola; Hahne, Jens C.

doi:10.1007/s11523-020-00717-x

Cited by 201 publications

(139 citation statements)

References 236 publications

(262 reference statements)

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“…Long non-coding RNAs (lncRNAs) are transcripts that are >200 nucleotides long (2). The regulatory RNA is abnormally expressed in various cancers, such as prostate cancer, liver cancer and lung cancer, making it an emerging diagnostic biomarker and therapeutic target (3)(4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Inhibiting proliferation and metastasis of osteosarcoma cells by downregulation of long non‑coding RNA colon cancer‑associated transcript 2 targeting microRNA‑143

Chen

et al. 2021

Oncol Lett

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Osteosarcoma is a malignant bone tumor, which has a high incidence in children and adolescents. However, the pathogenesis of osteosarcoma remains unclear. Long noncoding RNA (lncRNA) is a new potential therapeutic target and diagnostic biomarker for osteosarcoma. Hence, the present study aimed to explore the effect of lncRNA colon cancer-associated transcript (CCAT2) on osteosarcoma and its potential underlying mechanisms. For this purpose, the proliferation of osteosarcoma cells was measured using the CCK-8 assay. The scratch-wound and cell invasion assays were used to determine the migration and invasion of osteosarcoma cells, respectively. LncRNA CCAT2 and microRNA (miR)-143 binding sites were identified by the dual-luciferase reporter assay. RNA and protein expression levels were detected by reverse-transcription quantitative PCR and western blotting, respectively. Downregulation of lncRNA CCAT2 inhibited the proliferation, migration, and invasion of osteosarcoma cells. The findings also revealed that miR-143 bound directly to lncRNA CCAT2. The expression of miR-143 was upregulated by the knockdown of lncRNA CCAT2. Downregulation of the FOS-like antigen 2 was also observed after knockdown of lncRNA CCAT2. The function of lncRNA CCAT2 in osteosarcoma cells was attenuated by co-transfection with anti-miR-143 oligodeoxyribonucleotide. In conclusion, downregulation of lncRNA CCAT2 inhibited the proliferation and metastasis of osteosarcoma cells by targeting miR-143. lncRNA CCAT2 was identified as a potential target for osteosarcoma treatment.

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Section: Introductionmentioning

confidence: 99%

Inhibiting proliferation and metastasis of osteosarcoma cells by downregulation of long non‑coding RNA colon cancer‑associated transcript 2 targeting microRNA‑143

Chen

et al. 2021

Oncol Lett

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“…Therefore, investigations of the underlying mechanism of cervical cancer metastasis, including cell proliferation and invasion are urgent and could be helpful to improve the clinical outcomes of patients. Recent studies have shown that miRNAs or lncRNAs play an important regulatory role in a variety of physiological and pathological processes [ 21 , 22 ], including malignant tumors. In addition, miRNAs and lncRNAs are involved in the occurrence and metastasis of several cancers.…”

Section: Discussionmentioning

confidence: 99%

Linc00887 suppresses tumorigenesis of cervical cancer through regulating the miR-454-3p/FRMD6-Hippo axis

Li¹,

Wang²,

Zhi

et al. 2021

Cancer Cell Int

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Background Emerging evidence suggested that long intergenic noncoding RNA (lincRNA) 00887 (NR_024480) reduced the invasion and metastasis of non-small cell lung cancer by sponging miRNAs degradation. However, the role and regulatory mechanism of linc00887 in the progression of cervical cancer remain largely unknown. Methods In vivo or vitro, RT-qPCR assay was used to detect the expression of linc00887 in human normal (N = 30), cervical cancer tissues (N = 30), human normal cervical epithelial cells (Ect1/E6E7) and cervical cancer cell lines (HeLa, C33A). Then, CCK-8 and Transwell assays were used to examine cell proliferation and invasion when linc00887 was overexpressed or knocked down. In addition, bioinformatics, luciferase reporter gene and pull-down assays were used to predict and validate the relationship between linc00887 and miR-454-3p. Moreover, we detected the expression of miR-454-3p in Ect1/E6E7, HeLa and C33A cells when linc00887 was overexpressed or knocked down. Cell proliferation and invasion were also measured when pcDNA-linc00887 and miR-454-3p were transfected alone or together. Next, miR-454-3p target gene was predicted and validated by bioinformatics and luciferase reporter gene assays. Gain- and loss-of-function experiments were performed in HeLa cells to evaluate the effect of miR-454-3p or linc00887 on the expression of FERM domain containing protein 6 (FRMD6) protein and several key proteins in the FRMD6-Hippo signaling pathway. Results Linc00887 was downregulated in cervical cancer tissues or human cervical cancer cell lines (Hela, C33A) compared with normal tissues or cell lines. Overexpression of linc00887 inhibited proliferation and invasion HeLa and C33A cells, while linc00887 knockdown had the opposite effect. Linc00887 bound with miR-454-3p, and overexpression of miR-454-3p rescued linc00887-induced inhibition proliferation and invasion of HeLa cells. MiR-454-3p targeted and suppressed the expression of FRMD6, and linc00887 suppressed tumorigenesis of cervical cancer through activating the FRMD6-Hippo signaling pathway. Conclusions Linc00887, sponging miR-454-3p, inhibited the progression of cervical cancer by activating the FRMD6-Hippo signaling pathway.

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“…MiRNAs, as a kind of highly conserved short ncRNAs, have a length of 18–25 nucleotides, regulate the expression of many genes, and participate in the development of human cancer and drug resistance ( Poursheikhani et al, 2020 ; Ratti et al, 2020 ). miRNA-mediated autophagy ( Figure 5B ) has been found to play a role in chemoresistance in gastric cancer by regulating autophagy-related genes or signaling pathways ( Jamali et al, 2020 ).…”

Section: Dual Roles Of Autophagy In Chemoresistance Of Gastric Cancermentioning

confidence: 99%

The Role of Autophagy in Gastric Cancer Chemoresistance: Friend or Foe?

Tang

et al. 2020

Front. Cell Dev. Biol.

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Gastric cancer is the third most common cause of cancer-related death worldwide. Drug resistance is the main inevitable and vital factor leading to a low 5-year survival rate for patients with gastric cancer. Autophagy, as a highly conserved homeostatic pathway, is mainly regulated by different proteins and non-coding RNAs (ncRNAs) and plays dual roles in drug resistance of gastric cancer. Thus, targeting key regulatory nodes in the process of autophagy by small molecule inhibitors or activators has become one of the most promising strategies for the treatment of gastric cancer in recent years. In this review, we provide a systematic summary focusing on the relationship between autophagy and chemotherapy resistance in gastric cancer. We comprehensively discuss the roles and molecular mechanisms of multiple proteins and the emerging ncRNAs including miRNAs and lncRNAs in the regulation of autophagy pathways and gastric cancer chemoresistance. We also summarize the regulatory effects of autophagy inhibitor and activators on gastric cancer chemoresistance. Understanding the vital roles of autophagy in gastric cancer chemoresistance will provide novel opportunities to develop promising therapeutic strategies for gastric cancer.

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MicroRNAs (miRNAs) and Long Non-Coding RNAs (lncRNAs) as New Tools for Cancer Therapy: First Steps from Bench to Bedside

Cited by 201 publications

References 236 publications

Inhibiting proliferation and metastasis of osteosarcoma cells by downregulation of long non‑coding RNA colon cancer‑associated transcript 2 targeting microRNA‑143

Inhibiting proliferation and metastasis of osteosarcoma cells by downregulation of long non‑coding RNA colon cancer‑associated transcript 2 targeting microRNA‑143

Linc00887 suppresses tumorigenesis of cervical cancer through regulating the miR-454-3p/FRMD6-Hippo axis

The Role of Autophagy in Gastric Cancer Chemoresistance: Friend or Foe?

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